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Hepatopulmonary syndrome (HPS) is defined by liver disease, hypoxaemia, increase of alveolar-arterial gradient, when inhaling room air, and intrapulmonary vascular dilatation. Pathoanatomical substrate of intrapulmonary vascular dilatation consists of dilated precapillary network, direct arterio-venous communication and dilated pleural blood vessels, "pleural spiders" [2]. Recently, hepatopulmonary syndrome gained clinical significance. Deterioration of arterial oxygenation in patients with liver disease indicates a very poor prognosis, because of which there are suggestions to classify hepatopulmonary syndrome as a new indication of liver transplantation [4]. ⋯ It is supposed that approximately 50% of patients with indication for liver transplantation have some form of arterial oxygenation disorder and 13-47% of these patients may have HPS [6, 7]. In our study, HPS was diagnosed in 18% of patients. We explain this high incidence by the fact that our study included the patients with advanced liver cirrhosis (stages Child's B and C). In studies performed up to date, there was neither correlation between biochemical liver function parameters and intrapulmonary shunts, nor any strong relation between severity of hepatic failure and degree of hypoxaemia [12, 13]. We noticed no correlation between hepatic functions (synthetic, excretory, transaminases) and PaO2 and/or intrapulmonary shunts. Some authors suggested that ventilation-perfusion disorder (Va/Q) is an important cause of hypoxaemia in